Methods to Produce Brain Hyperthermia

Sharma, Hari Shanker

doi:10.1002/0471140856.tx1114s23

Cited by 19 publications

(15 citation statements)

References 54 publications

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“…To measure water content, after obtaining the wet weight, the samples were placed in an oven maintained at 90 °C for 72 h or until the last three dry weight measurements were constant. Water content was calculated according to the formula: wet weight‐dry weight/wet weight × 100 (Rapoport, 1976; Sharma, 2005a,b). To measure ions, the samples, after obtaining the dry weight, were heated at 550 °C for 24 h to produce ash.…”

Section: Methodsmentioning

confidence: 99%

Brain edema and breakdown of the blood–brain barrier during methamphetamine intoxication: critical role of brain hyperthermia

Kiyatkin

Brown

Sharma

2007

Eur J of Neuroscience

121

139

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To clarify the role of brain temperature in permeability of the blood-brain barrier (BBB), rats were injected with methamphetamine (METH 9 mg/kg) at normal (23 degrees C) and warm (29 degrees C) environmental conditions and internal temperatures were monitored both centrally (nucleus accumbens, NAcc) and peripherally (skin and nonlocomotor muscle). Once NAcc temperatures peaked or reached 41.5 degrees C (a level suggesting possible lethality), animals were administered Evans blue dye (protein tracer that does not normally cross the BBB), rapidly anaesthetized, perfused and had their brains removed. All METH-treated animals showed brain and body hyperthermia associated with relative skin hypothermia, suggesting metabolic activation coupled with peripheral vasoconstriction. While METH-induced NAcc temperature elevation varied from 37.60 to 42.46 degrees C (or 1.2-5.1 degrees C above baseline), it was stronger at 29 degrees C (+4.13 degrees C) than 23 degrees C (+2.31 degrees C). Relative to control, METH-treated animals had significantly higher brain levels of water, Na(+), K(+) and Cl(-), suggesting brain edema, and intense immunostaining for albumin, indicating breakdown of the BBB. METH-treated animals also showed strong immunoreactivity for glial fibrillary acidic protein (GFAP), possibly suggesting acute abnormality or damage of astrocytes. METH-induced changes in brain water, albumin and GFAP correlated linearly with NAcc temperature (r = 0.93, 0.98 and 0.98, respectively), suggesting a key role of brain hyperthermia in BBB permeability, development of brain edema and subsequent functional and structural neural abnormalities. Therefore, along with a direct destructive action on neural cells and functions, brain hyperthermia, via breakdown of the BBB, may be crucial for both decompensation of brain functions and cell injury following acute METH intoxication, possibly contributing to neurodegeneration resulting from chronic drug use.

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Section: Methodsmentioning

confidence: 99%

Brain edema and breakdown of the blood–brain barrier during methamphetamine intoxication: critical role of brain hyperthermia

Kiyatkin

Brown

Sharma

2007

Eur J of Neuroscience

121

139

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“…After visual inspection of the Evans blue, the samples were measured for radioactivity in a gamma counter. The leakage of tracers across the spinal cord was expressed as a percentage increase over blood concentration 29–31 …”

Section: Materals and Methodsmentioning

confidence: 99%

“…Spinal cord edema formation was calculated using water content determined from the difference between the wet and dry weights of the samples, as described earlier 32,33 . Volume swelling (%Ÿ) of the spinal cord was calculated from the difference between controls and injured water content according to the formula of Elliott and Jasper, 34 as described earlier 30–31 …”

Section: Materals and Methodsmentioning

confidence: 99%

A Select Combination of Neurotrophins Enhances Neuroprotection and Functional Recovery following Spinal Cord Injury

Sharma

2007

Annals of the New York Academy of Sciences

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Previously, we have shown that topical application of brain-derived neurotrophic factor (BDNF) or insulin-like growth factor 1 (IGF-1) given within 5 to 30 min after a focal trauma to the rat spinal cord attenuates spinal cord injury (SCI)-induced breakdown of the blood-spinal cord barrier (BSCB), edema formation, motor dysfunction, and cell injury. This investigation was undertaken to find out whether a combination of select neurotrophins (BDNF, glial cell line-derived neurotrophic factor [GDNF], neurotrophin 3 [NT-3], or nerve growth factor [NGF]) will further enhance the neuroprotective efficacy of growth factors in SCI. The neurotrophins (0.1-1 microg/10 microL in phosphate-buffered saline) were applied 30, 60, or 90 min after injury topically over the traumatized spinal cord either alone or in combination. The SCI was performed by making a unilateral incision into the right dorsal horn of the T10-T11 segment under Equithesin anesthesia. The rats were allowed to survive 5 h after trauma. Topical application of BDNF, GDNF, or NGF 30 min after SCI in high concentration (0.5 microg and 1 microg) significantly improved the motor functions and reduced the BSCB breakdown, edema formation, and cell injury seen at 5 h. These beneficial effects of neurotropins were absent when administered separately either 60 or 90 min after SCI. However, a combination of BDNF and GDNF (but not with NT-3 or NGF) given either 60 or 90 min after SCI significantly reduced the motor dysfunction and spinal cord pathology at 5 h. These novel observations suggest that a select group of neurotrophins in combination have potential therapeutic value for the treatment of SCI in clinical situations.

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“…To measure water content, after obtaining the wet weight, the samples were placed in an oven, maintained at 90 °C, for 72 h or until three dry weight measurements were constant. Water content was calculated according to the formula: wet weight-dry weight/wet weight × 100 [138,139]. To measure ions, after obtaining the dry weight, the samples were heated at 550 °C for 24 h to produce ash.…”

Section: Brain Water and Electrolyte Contentmentioning

confidence: 99%

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

Miclescu¹

2010

Acta Anaesthesiol Scand

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Although survival rates are increasing, brain injury continues to be a leading cause of death after cardiac arrest (CA). Permanent brain damage after CA is determined by limited tolerance to ischemia from CA and cardiopulmonary resuscitation (CPR), as well as the unique cerebral response to reperfusion after return of spontaneous circulation (ROSC). A major pathway leading to neurotoxic cascade and neuronal injury after CA involves the increased presence of reactive oxygen and nitrogen species generated during ischemia and reperfusion. The magnitude of cerebral oxidative injury induced by free radicals increased with the duration of CA (Paper I). Nitric oxide (NO), a free radical responsible for the formation of reactive nitrogen species, is increased during global ischemia from CA and reperfusion (Paper IV). Hypothetically, the administration of a drug that counteracts the overproduction of NO and also acts as a scavenger of oxygen free radicals might be warranted in order to reduce the damage caused by nitrosative and oxidative stress. For these purposes we used methylene blue (MB), an old dye that has been used in medicine for almost half a century, and an experimental pig model of 20 min of ventricular fibrillation (VF) to reflect a clinical scenario of ischemia/reperfusion injury. Administration of MB added to a hypertonic-hyperoncotic solution (MBHSD) that was started during CPR and continued for 50 min after ROSC increased short-term survival by decreasing myocardial damage, as well as cerebral peroxidation and inflammatory injury (Paper II). Immunostaining of cerebral tissue collected at different time points after CA and ROSC (Paper IV) provided experimental evidence that cortical blood-brain barrier (BBB) disruption begins as early as during the initial phase of untreated as well as treated CA. The results indicated that MB administration reduced the neurologic injury and BBB disruption considerably, but did not reverse the ongoing detrimental processes. The demonstrated positive effects of MB were related to a decrease of nitrite/nitrate tissue content, and thus to a decrease of excess NO due to the MB inhibitory effects on NOS isoforms. A mixture of MB in hypertonic sodium lactate (MBL) was investigated to facilitate administration of MB in "the field." Based on findings that MBL cardio-and neuroprotective properties were similar to those of MBHSD, there is reason to believe that the use of MBL might be extended during ongoing CPR and after ROSC (Paper III). It would therefore make sense to try using MB as a pharmacological neuroprotectant during or after clinical CPR in order to expand the temporal therapeutic window before other measures for neuroprotection such as hypothermia are available. Keywords: Cardiac arrest, cardiopulmonary resuscitation, reperfusion injury, methylene blue, nitric oxide, nitric oxide synthases, blood-brain barrier

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Methods to Produce Brain Hyperthermia

Cited by 19 publications

References 54 publications

Brain edema and breakdown of the blood–brain barrier during methamphetamine intoxication: critical role of brain hyperthermia

Brain edema and breakdown of the blood–brain barrier during methamphetamine intoxication: critical role of brain hyperthermia

A Select Combination of Neurotrophins Enhances Neuroprotection and Functional Recovery following Spinal Cord Injury

Cerebral protection in experimental cardiopulmonary resuscitation (with special reference to the effects of methylene blue)

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